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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Role of neuronal nitric oxide synthase in Dahl salt-sensitive hypertension.

The goal of this study was to determine the role of neuronal nitric oxide synthase (nNOS) in the arterial pressure, renal hemodynamic, and renal excretory changes that occur in Dahl salt-resistant (DR) and salt-sensitive (DS) rats during changes in Na intake. Fifty-three DR and DS rats/Rapp strain of 7 to 8 weeks of age with indwelling arterial and venous catheters were subjected to low (0.87 mmol/d) or high (20.6 mmol/d) Na intake beginning 2 days before the start of the control period. Measurements were made during a 5-day control period followed by a 5-day period of nNOS inhibition with intravenous 7-nitroindazole (7NI, 1.67 mg. kg-1. h-1) or vehicle infusion. After 5 days of 7NI, mean arterial pressure increased to 120+/-6% control in the DR-high Na, 7NI rats compared with 98+/-1% control (P<0.05) in the DR-high Na alone rats. After 5 days of 7NI, DS-high Na rats, which had a control arterial pressure 31 mm Hg higher than the comparable DR rats, increased their arterial pressure to 114+/-3% control, which was not significantly different from the DS-high Na alone pressure of 110+/-2% control. No significant changes occurred in glomerular filtration rate, effective renal plasma flow, urinary Na excretion, or urine volume because of 7NI. However, plasma renin activity decreased significantly in DR and DS rats on low Na intake with 7NI infusion. The data demonstrate that the highly salt-resistant DR rat became salt-sensitive during nNOS inhibition with 7NI. However, the arterial pressure of the DS rat was not affected by 7NI. This suggests that nitric oxide produced by nNOS in the DR rat normally helps to prevent salt-sensitive hypertension and that low functional levels of nNOS in the DS rat may contribute to its salt-sensitivity.[1]


  1. Role of neuronal nitric oxide synthase in Dahl salt-sensitive hypertension. Tan, D.Y., Meng, S., Manning, R.D. Hypertension (1999) [Pubmed]
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